hVEGF-IN-1

1637443-98-1

C34H43N7O2

DMSO : 25 mg/mL (42.97 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble)

Protein Tyrosine Kinase/RTK

hVEGF-IN-1 represses human VEGF-A translation and shows antitumor activity. IC50 & Target: VEGFR^[1] In Vitro: hVEGF-IN-1 shows a significant specific interaction with the G-rich region within the 5?- untranslated regions (5?-UTR) of hVEGF-A mRNA and destabilizes the Gquadruplex structure. hVEGF-IN-1 binds to the IRES-A (WT) with a K_d of 0.928 uM and binds to the hairpin DNA with a K_d of 21.2 uM. The G-rich sequence G774-G790 within the IRES-A of hVEGF-A’s 5?-UTR has been shown to be critical for the translation initiation activity of IRES-A. hVEGF-IN-1 hinders BG4 from binding to the IRES-A RNA G-quadruplex in cells. hVEGF-IN-1 down-regulates hVEGF-A’s translation via the G-quadruplex within IRES-A mRNA. hVEGF-IN-1 treatment reduces MDA-MB- 231 cell migration to approximately 25%^[1]. In Vivo: Tumor bearing mice treated with hVEGF-IN-1 have an average tumor volume of less than 300 mm³. The tumor weight in the presence of hVEGF-IN-1 reduces around 60.1% to a final weight of 0.18 g. No significant change in body weight is observed during the treatment^[1].